title: In vitro TNF-α- and noradrenaline-stimulated lipolysis is impaired in adipocytes from growing rats fed a low-protein, high-carbohydrate diet.
abstract: The aim of this study was to investigate tumor necrosis factor alpha (TNF-α)- and noradrenaline (NE)-stimulated lipolysis in retroperitoneal (RWAT) and epididymal (EAT) white adipose tissue as a means of understanding how low-protein, high-carbohydrate (LPHC) diet-fed rats maintain their lipid storage in a catabolic environment (marked by increases in serum TNF-α and corticosterone and sympathetic flux to RWAT and EAT), as previously observed. Adipocytes or tissues from the RWAT and EAT of rats fed an LPHC diet and rats fed a control (C) diet for 15 days were used in the experiments. The adipocytes from both tissues of the LPHC rats exhibited lower TNF-α- stimulated lipolysis compared to adipocytes from the C rats. The intracellular lipolytic agents IBMX, DBcAMPc and FSK increased lipolysis in both tissues from rats fed the C and LPHC diets compared to basal lipolysis; however, the effect was approximately 2.5-fold lower in adipocytes from LPHC rats. The LPHC diet induced a marked reduction in the β3 and α2-AR, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) content in RWAT and EAT. The LPHC diet did not affect TNF-α receptor 1 content but did induce a reduction in ERK p44/42 in both tissues. The present work indicates that RWAT and EAT from LPHC rats have an impairment in the lipolysis signaling pathway activated by NE and TNF-α, and this impairment explains the reduced response to these lipolytic stimuli, which may be fundamental to the maintenance of lipid storage in LPHC rats.
authors.affiliation: Department of Chemistry, Federal University of Mato Grosso, Cuiabá, MT, Brazil.
authors.forename: Daniel D S
authors.initials: DD
authors.lastname: Feres
authors.forename: Maísa P
authors.initials: MP
authors.lastname: Dos Santos
authors.forename: Samyra L
authors.initials: SL
authors.lastname: Buzelle
authors.forename: Mayara P
authors.initials: MP
authors.lastname: Pereira
authors.forename: Suélem A
authors.initials: SA
authors.lastname: de França
authors.forename: Maria A R
authors.initials: MA
authors.lastname: Garófalo
authors.forename: Cláudia M B
authors.initials: CM
authors.lastname: Andrade
authors.forename: Mendalli
authors.initials: M
authors.lastname: Froelich
authors.forename: Fhelipe J S
authors.initials: FJ
authors.lastname: de Almeida
authors.forename: Danúbia
authors.initials: D
authors.lastname: Frasson
authors.forename: Valéria E
authors.initials: VE
authors.lastname: Chaves
authors.forename: Nair H
authors.initials: NH
authors.lastname: Kawashita
mesh_terms: D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D052436:Adipose Tissue, White / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D003994:Bucladesine / Q000494:pharmacology; D004032:Diet; D018753:Diet, Protein-Restricted; D004040:Dietary Carbohydrates / Q000494:pharmacology; D008049:Lipase / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism; D022702:Receptors, Adrenergic, beta-3 / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D002787:Sterol Esterase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000494:pharmacology*; D000217:Acyltransferases
chemical_list: D015056:1-Methyl-3-isobutylxanthine; D003994:Bucladesine; D004040:Dietary Carbohydrates; D008049:Lipase; D009638:Norepinephrine; D018341:Receptors, Adrenergic, alpha-2; D022702:Receptors, Adrenergic, beta-3; D018124:Receptors, Tumor Necrosis Factor; D002787:Sterol Esterase; D014409:Tumor Necrosis Factor-alpha; C571275:PNPLA2 protein, rat; D000217:Acyltransferases